surgery complications of acute myocardial...

SYMPOSIU1MMyocardial Infarction 1972

(Part 6)

Surgery for Complications of AcuteMyocardial Infarction

By ELDRED D. MUNDTH, M.D., MORTIMER J. BUCKLEY, MI.D.,

WILLARD M. DAGGETT, M.D., CHARLES A. SANDERS, M.D.,

AND W. GERALD AUSTEN, M.D.

W ITH THE GREATER availability ofwell-equipped and well-staffed coro-

nary care units, death from arrhythmiascomplicating myocardial infarction has be-come less common.' This has been a result ofimproved methods of patient monitoring,earlier diagnosis of arrhythmias, and prompttreatment.2 3 Death from myocardial infarc-tion at present is more commonly a result ofcardiogenic shock or refractory cardiac fail-ure." 3-5 The mechanical complications ofmyocardial infarction, including rupture of theinterventricular septum, papillary muscle rup-ture, and acute left ventricular aneurysm,although uncommon, are associated wih ahigh mortality rate.Concomitant with the development of an

accurate and safe method of selective cine-coronary arteriography6 for the diagnosis ofcoronary artery disease, effective surgicalprocedures for direct coronary arterial revas-cularization have evolved.7-10 Despite animpressive volume of patients undergoingelective revascularization, urgent myocardial

From the Department of Surgery and Medicine,Harvard Medical School and the General Surgical andMedical Services, Massachusetts General Hospital,Boston, Massachusetts.

Supported by U. S. Public Health Service GrantsHE-12489 and HE-06664 and Contract 43-67-1443.

revascularization, infaretectomy, repair ofventricular septal defect, or mitral valvereplacement in patients with complications ofacute myocardial infarction has been infre-quent. Until recently, surgery for the compli-cations of acute myocardial infarction lessthan 4 weeks from the time of the infarct hasbeen associated with a near-prohibitive mor-tality."-'.' After an interval of 4 weeks ormore, revascularization or correction of me-chanical defects resulting from infarction havebeen associated with reasonably good clinicalresults.'4 16 The latter group obviously in-cludes only those patients remaining hemody-namically stable and surviving 4 weeks ormore after myocardial infarction. However,the majority of patients dying of complica-tions of acute myocardial infarction do sowithin 2 weeks of the time of infarction.'7' 18

Increasing clinical application of mechani-cal circulatory assistance, early diagnosticstudy by cardiac catheterization and cinecoro-nary angiography, and, recently, acute surgi-cal intervention have resulted in a significantsalvage of patients within 4 weeks of the timeof infarct. The present discussion will belimited primarily to patients in this category.

Cardiogenic Shock

Cardiogenic shock, or left ventricular powerfailure, is at present the complication of acute

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myocardial infarction which most commonlyresults in death.4 17. 19 Most recent series havereported an overall mortality from acutemyocardial infarction in the range of 30 to40%, with approximately 20% of the deathsoccurring outside of the hospital.17 In acooperative study from nine coronary careunits the mortality of acute myocardialinfarction in 2842 patients ranged from 14 to30% with an average of 25%.1 The major causeof death was pump failure, or cardiogenicshock, which was associated with a mortalityof 80-90% once shock became clinically mani-fest.The initial physiologic insult of a major

myocardial infarction results in a decrease inleft ventricular function manifested by a fallin cardiac output and arterial perfusionpressure. The latter results in diminishedcoronary perfusion, which further contributesto the functional deficit of the ischemicmyocardium. Thus, a vicious cycle of eventsmay ensue, which often results in extension ofthe original infarct and progressive leftventricular power failure. Left ventricularfunction is not only adversely influenced bythe actually infarcted myocardium, but alsoby the presence of a functionally compro-mised ischemic periinfarction zone myocar-dium. Schelbert et al.20 and Hood et al.2' haveshown that myocardial contractility is de-pressed in ischemic areas of the left ventriclebut not eliminated unless cell death hasoccurred. Myocardial contractility in ischemicareas of the left ventricle can be temporarilyimproved with administration of inotropicagents such as isoproterenol, but eventually atthe expense of increasing the area of myocar-dial injury.22 24 The cause of this increasedmyocardial injury is the increased oxygenrequirement of the ischemic myocardiuminduced by the inotropic agent, in a situationwhere oxygen delivery cannot be enhanced.Hypotension and reduction of coronary perfu-sion pressure also result in further depressionof myocardial function in ischemic zones andlead to extension of the area of injury.25' 26Particularly at low coronary perfusion pres-sures, left ventricular function is coronary

perfusion-pressure dependent.2' 28 These ob-servations are of obvious clinical importance.Thus, it is essential to maintain an adequatecoronary perfusion pressure in the cardiogenicshock patient, but it is desirable to achievethis without increasing myocardial oxygenrequirements, as occurs with the administra-tion of most catecholamines. In experimentalstudies of cardiogenic shock, Rona, Kahn, andChappel29 demonstrated the development offocal areas of myocardial necrosis in animalstreated with catecholamines. Focal areas ofmyocardial necrosis resulting from the hem-orrhagic shock state were shown by Gomez etal.25 to occur despite maintenance of normalcoronary blood flow. This may be blocked byadministration of pronethalol as shown byEntman et al.30 Clinical studies of patients incardiogenic shock have shown that a pressorresponse is observed with administration ofeither alpha- or beta-adrenergic catechola-mines, but the mortality rate is not significant-ly influenced.4 5 24 3' Potential adverse effectsof catecholamine administration are difficultto ascertain since the overall mortality rateregardless of therapy has been in the range of80to 90%.1 3. 4The clinical criteria for definition of car-

diogenic shock are obviously important ifaccurate assessment of the effectiveness ofvarious forms of therapy is to be achieved.The incidence of shock complicating acutemyocardial infarction and the results oftherapy differ in various series primarilybecause of differences in definition of theshock state.17 It is not uncommon for shock toappear early in the clinical course of a patientwith an acute infarct but to subside within 1-3hours with supportive measures only. Shockpersisting longer than 1-3 hours is the primaryconcern of this discussion. The criteria forcardiogenic shock, as established by Myocar-dial Infarction Research Unit (MIRU) cen-ters across the country, include: (1) arterialblood pressure less than 90 mm Hg, (2)oliguria, with urine output less than 20ml/hour, and (3) systemic manifestations ofshock including peripheral vasoconstriction,mental confusion, or obtundation. Further

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subelassification of the degree of severity ofshock based upon hemodynamic criteria hasbeen useful in analyzing the results of therapy.The product of the cardiac index and mean

arterial pressure (Cl x AP) yields a roughindex of ventricular function. When thisproduct is less than 120, the degree of shock iscategorized as severe, class 4. When theCI x AP product is greater than 120, but thePCWP is elevated above 20 mm Hg, thedegree of shock is categorized as class 3. Class2 shock exists when the clinical criteria forshock are present but the CI x AP product isgreater than 120 and the PCWP is less than20 mm Hg.On the basis of a clinical study of 73

patients in cardiogenic shock, Scheidt, As-cheim, and Killip4 found that there were no

common predisposing factors such as a

previous infarct, previous angina, hyperten-sion, or cardiac failure. In addition, theseauthors found no consistent correlation withthe development of cardiogenic shock and thelocation of the infarct or duration of time fromthe onset of symptoms. Page et al.3 however,found in their review of 20 patients dying ofcardiogenic shock that 65% had a previousinfarct, and the lower anterior wall and apex

of the left ventricle were involved in allpatients. A common finding in all studies was

that the area of left ventricular loss was 40% or

greater. In the study 'by Scheidt et al.' theSGOT was found to be markedly elevated(> 400 mg/ 100 ml) more commonly in shockpatients. Although a hemodynamic response

to norepinephrine, aramine, or isoproterenolwas observed in nearly all patients, there was

no significant difference in mortality. In thisstudy, where the average cardiac index was

1.1 liters/min/m2, the mortality was 50% at

10.2 hours after the onset of shock and 86%overall.Treatment of the shock syndrome must be

i'ndividualized. In order to assess the moment-to-moment clinical status of a patient in shockand to determine the effectiveness of therapy,careful physiologic monitoring is essential.33The pharmacologic treatment of cardiogenicshock has not been overly effective.4 24,31

Although catecholamine administration usual-ly results in an elevation of arterial pressure

and cardiac index, it may cause further injuryto the ischemic myocardium as previouslydiscussed. When the shock state is associatedwith a CI > 2 liters/min/m2 and a low totalperipheral vascular resistance (mean AP/CI)it may be desirable to increase peripheralvascular tone with an alpha-adrenergic drugsuch as norepinephrine or metaraminol. Ob-viously, this increases left ventricular afterloadand left ventricular work. Arrhythmias whichresult in a reduction in cardiac output or inthe efficiency of atrioventricular transportmust be treated promptly. Atrial or sequentialatrioventricular pacing, not infrequently, isthe only therapeutic measure required tobring the patient out of shock. Support of an

adequate blood volume as' determined by leftand right heart filling pressures is alsoessential to maintain an optimal cardiacoutput. If the patient remains in cardiogenicshock despite these measures, circulatoryassistance should be considered (table 1).There are several systems clinically avail-

able for mechanical circulatory assistance,each with its own advocates.3438 Presently,the most extensive and successful clinicalexperience with mechanical circulatory assis-tance has been with the intraaortic balloonpump. The physiologic benefits of circulatory

Table 1Therapeutic Measures for Treatment of Cardiogenic Shock

1. Supportive Oxygen, morphine, blood volume adjustment,correction or acidosis

2. Electrical pacing technics Atrial or sequential atrioventricular pacing3. Pharmacologic Antiarrhythmic druigs, catecholamines, digitalis4. Circulatory assistance

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assistance to the ischemic injured heart arediscussed elsewhere in this symposium.3Clinical hemodynamic evaluation of circula-tory assistance with intraaortic balloon pump-ing (IABP) for the treatment of patients incardiogenic shock has demonstrated a signifi-cant reduction in left ventricular peak systolicpressure, a reduction in left ventricular end-diastolic pressure, and significant improve-ment in cardiac output. Although there havebeen a number of striking results, the acutemortality of patients treated by IABP assis-tance has remained in the range of 80%. Mostof the patients treated by this means, how-ever, were in severe class 4 cardiogenic shock.Although a concomitant control group ofsimilar patients treated conventionally was notobserved, it is probable that the expectedmortality of this group of patients treatedconventionally would approach 100%.Braunwald et al.27 have suggested that the

fate of a patient with myocardial infarctionand cardiogenic shock depends upon a bal-ance between the myocardial oxygen require-ments needed to maintain an adequatecirculation and the capacity for oxygendelivery to the ischemic myocardium. Anotherobvious factor is the extent of the irreversiblyinjured myocardium. In some instances, thetotal left ventricular area irreversibly involvedmay be too extensive for recovery with anymode of therapy short of cardiac replacement.In many instances, as suggested by clinicopa-thologic studies previously discussed, leftventricular wall loss appears to be progressiveduring the early course of infarction. In viewof this concept and with the development ofeffective methods for direct coronary arterialrevascularization, the possibility of acutemyocardial revascularization reversing cardio-genie shock became a therapeutic potentialrequiring evaluation.Segmental myocardial ischemia has been

shown to result in a reduction in contractilityin the ischemic zone which can be reversed byrestoring adequate coronary perfusion.39 40 Aspreviously noted, persistence of an acutelyischemic periinfarction zone leads to eventualcell death and extension of the infarction.

Prompt institution of mechanical circulatoryassistance in the clinical setting may preventthis course by reducing the left ventricularwork requirement and associated oxygendemand of the ischemic zone of myocardium.Mechanical circulatory assistance, if promptlyinstituted, may prevent extension of theinfarcted zone, but since the relative inade-quacy of myocardial oxygen supply persists,hemodynamic recovery may not be adequatewhen circulatory assistance is eventuallyterminated. Although Jacobey et al.4' suggest-ed that brief periods of counterpulsationopened intercoronary collaterals in the acutelyischemic heart enabling hemodynamic recov-ery after only a brief period of circulatoryassistance, subsequent clinical experience hasnot corroborated this. The development ofintercoronary collaterals on the basis ofexperimental studies normally requires weeksto months in response to the stimulus ofmyocardial ischemia.42 The combination ofprompt institution of mechanical circulatoryassistance and direct coronary artery revas-cularization thus emerged as a possible newmode of therapy for the patient with refrac-tory cardiogenic shock. Direct coronary arteri-al revascularization, by providing improvedperfusion of the ischemic periinfarction zoneof myocardium, may allow sufficient recoveryof left ventricular function for survival.

Despite the critically ill status of patientswith an acute myocardial infarction, coronaryangiographic study can be performed withrelative safety.43 The patient in cardiogenicshock presents a considerable risk for anydiagnostic study. However, Leinbach, et al.44demonstrated that complete evaluation of theshock patient can be safely achieved, includ-ing coronary arteriography and left ventricu-lography, with the protection of intraaorticballoon pump assistance.A number of centers have reported series of

patients undergoing emergency revasculariza-tion for impending or evolving myo-cardial infarction with generally excellentresults.'2 4 46 In none of these series did thepatients have associated shock except in onepatient who died at the time of surgery,


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reported by Scanlon et al.12 Our experiencehas indicated that the combination of circula-tory assistance with acute revascularizationsalvaged a significant number of patients inrefractory cardiogenic shock."6 33 47, 48 Therole of infarctectomy in the management ofthese patients is not yet clarified. Heimbeck-er's original reports of experimental studiesevaluating the efficacy of infarctectomy forthe treatment of acute myocardial infarctionwere encouraging.49 Their studies indicatedthat acute infarctectomy facilitated defibrilla-tion and resuscitation of canine hearts subject-ed to sudden ligation of the left anteriordescending coronary artery. The clinical ap-plication of the procedure, however, wascombined with closure of a ventricular septaldefect in three patients, which undoubtedlycontributed to their left ventricular functionalimpairment preoperatively. Glass et al.50 andJude5" have confirmed the experimentalstudies of Heimbecker, showing an improve-ment in the ability of the heart to bedefibrillated and an increase in cardiac outputwith resection of infarcts less than 30% of theleft ventricular wall. Resection of largerportions of the ventricular wall resulted in nosurvival. In a careful experimental studycomparing infarctectomy with J2 hour ofcirculatory assistance with cardiopulmonarybypass, Danielson, Resnicoff, and DeWeese'2found that there was no improvement in leftventricular power, arrhythmia control, orsurvival with infarcts greater than 13% of theleft ventricular total weight, whether treatedby infarctectomy or a brief period of circula-tory assistance. In a theoretic analysis basedupon the left ventricle considered as a sphere,Klein et al.53 concluded that the Starlingmechanism would fail with resection ofgreater than 20-25% of the left ventricularsurface area.

Clinical experience with acute infarctectomyless than 3-4 weeks following myocardialinfarction has been limited. Isolated reports ofsuccess following infarctectomy have been, forthe most part, in association with closure of asignificant ventricular septal defect.49 Thelargest single experience with both infaretec-Circulation, Volume XLV, June 1972

tomy and revascularization is that from theMassachusetts General Hospital.'6 33, 48As yet, no clear-cut criteria for selection of

patients for surgery has evolved, but certaingeneral guidelines have been established.When cardiogenic shock is profound orpersists for more than 1-2 hours after com-mencing general supportive care, circulatoryassistance should be considered. It is quiteclear from the experience with intraaorticballoon pump assistance that the maximumhemodynamic benefit is attained within 24-48hours of circulatory assistance.33 If, at thattime, hemodynamic studies without circula-tory assistance indicate a cardiac index of lessthan 2 liters/min/m2 or a pulmonary capillarywedge pressure of over 20 mm Hg, it isunlikely that the patient will ultimatelyrecover, in spite of continued circulatoryassistance. Urgent coronary angiographyshould usually be advised and surgery consid-ered if a surgically remediable situationexists.33 47" Criteria for establishment of asurgically remediable situation have beendifficult to establish. Of those patients operat-ed upon who failed to survive surgery,pathologic examination revealed left ventricu-lar wall loss of over 60% in most. It is quiteapparent that a number of patients withcardiogenic shock will have such extensivemyocardial loss that revascularization and/orinfarctectomy could not be effective. Carefulanalysis of the hemodynamic and angiograph-ic findings in the 16 patients undergoingsurgery did not reveal any obvious commondenominator in terms of patient selection.However, several findings appeared to berelative contraindications to surgery: (1)chronicity of clinical course; (2) poor or noresponse to inotropic agents; (3) severehypokinesia or akinesia involving greater than60% of the left ventricle; (4) inadequatecoronary vessels distally for bypass; and (5)avascularity of hypokinetic areas of leftventricle adjacent to the infarct.The decision as to the need for infarctec-

tomy in addition to revascularization has beenmade at the time of surgery. We presently feelthat several factors favor infaretectomy: (1)

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the presence of a large paradoxically bulginginfarct or acute aneurysm which appears tointerfere with left ventricular dynamics; (2)thinned-out necrotic infarct where ruptureappears imminent; or (3) a localized infarctassociated with recurrent ventricular arrhyth-mias.

It has been evident from our experiencethat mechanical circulatory assistance wasessential to the successful management of thesurviving patients. The prompt institution ofintraaortic balloon pump assistance preventedcontinued hemodynamic deterioration or ex-tension of the infarct, enabled safe completeangiographic study in each case, and facilitat-ed management of the patient both duringsurgery and after operation. The effect ofcoronary arterial revascularization on leftventricular function was immediately ap-parent in surviving patients. Visibly im-proved left ventricular contractility in thesepatients was associated with a significantimprovement in left ventricular hemodynam-ics in the early postoperative period. It isapparent from this experience that directcoronary arterial revascularization has thepotential of improving left ventricularfunction and reversing cardiogenic shockassociated with myocardial infarction in care-fully selected patients.33

Rupture of the Ventricular SeptumRupture of the ventricular septum is a

relatively uncommon complication of myocar-dial infarction. The incidence has beenreported in the range of 0.5 to 1% and accountsfor about 2% of all deaths following myocar-dial infarction.17Rupture of the ventricular septum usually

occurs in the lower septum associated with ananteroseptal infarct.17 Swithinbank, in a re-view of 113 cases, found 66% involving the lowseptum and 17% involving the posteriorseptum.54 This complication occurs mostcommonly in the first week after infarctionand clinically is characterized by a suddendeterioration in the patient's condition. Theleft-to-right shunt produced by the defectprecipitates severe biventricular failure in an

already compromised heart. Cardiogenicshock also may develop in association withincreasing failure. The mortality of thiscomplication is extremely high: 24% die within24 hours, 87% within 2 months, and over 90% at1 year.55The diagnosis of this complication of acute

myocardial infarction can be suspected whenthere is a sudden deterioration in the clinicalcourse of a patient associated with the abruptonset of a harsh systolic murmur at the leftsternal border. It is difficult clinically todistinguish rupture of the ventricular septumfrom dysfunction or rupture of the papillarymuscle and acute mitral regurgitation.15' 17Cardiac catheterization is necessary to estab-lished the diagnosis definitely.The feasibility of surgical repair has been

firmly established.14 Earlier experience indi-cated that successful surgical repair was muchmore likely beyond 4 weeks from the time ofperforation.13 14 Attempts at surgical repairless than 2 weeks following the developmentof perforation were associated with an ex-tremely high mortality. However, statisticshave demonstrated that 24% of patients withthis complication die within 24 hours and 65%within 2 weeks from the time of septalrupture.55 Interest in attempting closure of aseptal defect in the acute postinfarct periodwas stimulated by the report of Cooley et al.56in 1959 of a patient undergoing patch closure1 day following rupture of the septum. Thepatient survived acutely, but succumbed 8weeks postoperatively. Autopsy demonstrateda residual defect at the edge of the patch.Heimbecker49 and associates in 1967 first

reported successful closure of a septal defectin the acute postinfarct period combininginfarctectomy with closure of the septalperforation. The patient succumbed 1 monthlater of a complication of tracheostomy.Subsequently Stinson et al.57 Lajos et al." andDaggett et al.58 reported successful long-termsurvivals in three patients operated upon 9days, 5 days, and 3 days after septal rupture.From the accumulated earlier experience itwas apparent that an operative approachthrough a right ventriculotomy resulted in an


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overwhelming burden to the already compro-inised right ventricle.'6 8 Since the majorityof acquired septal perforations occur low inthe septum associated with a low anteroseptalor posteroseptal infarct, surgical closure of thedefect is usually feasible through a leftventriculotomy in the infarcted area.16 Resec-tion of the infarct, which, in some cases is anacute left ventricular aneurysm, may offerfurther hemodynamic benefit to left ventricu-lar function. Buckley et al.16 have recentlyreported four survivors of five patients operat-ed upon less than 10 days following septalrupture, using this approach. The averagefollow-up of these patients is 14 months, andall four are clinically well. Although this smallexperience has been encouraging, it is obviousthat the risk of surgery in the acute postinfarctperiod is high. Every attempt should be madeto support the patient medically until furthertime has elapsed, if it is at all possible. Clinicalexperience has been excellent with electiveclosure of acquired ventricular septal defects 8weeks to 6 months after an acute myocardialinfarction.14' 16 Although there are a fewreported long-term survivors of this complica-tion of myocardial infarction who have notundergone surgery, the majority who surviveinitially remain in a severely compromisedfunctional status until the septal defect issurgically closed.'17 18The question as to whether these patients

should have coronary arterial revasculariza-tion in addition to closure of the septal defectis not yet fully answered. In those patientswith acute refractory clinical deterioration lessthan 2 weeks from the time of septal rupture,the existence of a left-to-right shunt (Qp/Qs)of greater than 3:1 is probably a sufficienthemodynamic reason for their deterioration.In this situation, closure of the defect througha left ventriculotomy combined with infarctec-tomy is probably the procedure of choice. Inthe clinical situation where the left-to-rightshunt is marginal and left ventricular powerfailure appears to be the dominant hemody-namic deficit, direct coronary arterial revascu-larization probably should be combined withthe former procedure. This presupposes recog-Circulation, Volume XLV, June 1972

nition of this at the time of cardiac catheter-ization so that selective coronary angiographyand left ventriculography can be carried out.These basic guidelines probably also apply tothe consideration of surgery in patients whohave survived with medical support for longerthan 4-8 weeks following infarction and septalrupture. There may be a stronger indicationfor complete study including coronary arteri-ography and left ventriculography at thisstage since it carries much less risk and allowsa more complete evaluation of the patient. Asin patients with a chronic left ventricular an-eurysm following myocardial infarction, manycardiac surgeons and cardiologists wouldadvise coronary arterial revascularization inaddition to correction of the mechanicaldefect, particularly if there is significantdisease in major vessels not anatomically orfunctionally related to the area of themechanical defect.59

Papillary Muscle RuptureRupture of a papillary muscle resulting in

severe mitral regurgitation is a relatively rarecomplication of myocardial infarction, ac-counting for approximately 1% of deaths frominfarction.'7' 60 The location of the infarct isposterior in the majority of reported caseswith involvement of the posterior papillarymuscle.60 Disruption of the papillary muscleallows prolapse of the corresponding mitralvalve cusp during ventricular systole resultingin severe mitral valve incompetence. Thedevelopment of severe mitral regurgitationassociated with an already functionally com-promised left ventricle in the acute postinfarctperiod results in abrupt clinical deteriorationcharacterized by intractable left ventricu-lar failure and frequently, cardiogenicshock.'7, 18, 60 The mortality of this complica-tion has been reported as 70% within 24 hoursof the development of the murmur and near90% within 2 weeks.60

Papillary muscle rupture is usually charac-terized by the sudden development of a loudapical systolic murmur associated with abruptclinical deterioration 2-10 days after infarction.Papillary muscle rupture may be difficult to

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differentiate from rupture of the ventricularseptum in this setting, and cardiac catheteriza-tion is necessary to establish the definitivediagnosis. In the critically ill patient, rightheart catheterization, with measurement ofright ventricular oxygen content and pulmo-nary capillary wedge pressure, often is suffi-cient to establish the diagnosis.15 Papillarymuscle dysfunction due to infarction of themuscle can also produce severe mitral regurgi-tation in the early postinfaret period.61 Themurmur of mitral regurgitation and clinicaldeterioration may develop more slowly withthis entity but the hemodynamic effect issimilar.

Successful surgical repair of this mechanicaldefect complicating myocardial infarction wasfirst reported by Austen et al.6i in 1965. In thiscase, mitral valve replacement was carried out2J months following infarction. Subsequently,Austen and associates reported four survivorsin five patients undergoing mitral valvereplacement for treatment of this complica-tion. The four survivors were operated upon2-14 months after infarction. The one patientoperated upon less than 2 weeks aftermyocardial infarction failed to survive sur-gery. Similar experience was reported byCohen et al.63 Although Horlich et al.04reported success with suture reattachment ofthe ruptured papillary muscle and plication ofthe mitral annulus, many surgeons prefervalve replacement over direct suture repair ofthe friable infarcted papillary muscle.'5)

Since the majority of patients with thiscomplication become moribund with leftventricular failure and die within 24 hours or,at most, within 1-2 weeks, surgical repairfrequently must be undertaken in the acutepostinfarct period. In a recent report Buckleyet al.'" reported two survivors of four patientsoperated upon with mitral valve replacementwithin 2-10 days following the acute infarct.In comparison, 15 of 18 patients undergoingmitral valve replacement 3-7 months followinginfarction are surviving and clinically well. Aruptured papillary muscle was found in 10 in

this group and eight had dysfunction of afibrotic papillary muscle.

It is apparent from accumulated experiencethat the chance for survival with surgery isimproved when several weeks or months haveelapsed from the time of infarction. As ageneral guideline, vigorous supportive medicaltherapy is continued in the early postinfarctperiod as long as the patient improves orremains stable with an adequate hemody-namic status. Although the patient mayremain sufficiently stable clinically to delaysurgery, it is unusual for functional recoveryto be sufficient enough to be able to avoidsurgery.'7 18, 60 Clinically the patient presentswith the manifestations of severe mitralregurgitation with additional compromise ofleft ventricular function due to ischemicmyocardial disease. Frequently, a patient whodevelops rupture of a papillary muscle in theacute postinfarct period fails to respondadequately to vigorous supportive medicalcare. It is imperative to proceed urgently withcardiac catheterization and to define thehemodynamic diagnosis. In the patient whogoes into severe left venitricular failure,pulmonary edema, and shock, it may benecessary to initiate prompt circulatory assis-tance to attain some degree of cardiovascularstabilization in order to proceed with diagnos-tic study and facilitate preparationi of thepatient for surgery. In this clinical setting,complete hemodynamic evaluation is usuallyadvisable, including coronary arteriographyand left ventriculography in addition to rightheart catheterization. For significant salvageof the patient in cardiogenic shock, coronaryarterial revascularization and/or infaretec-tomy may be required in addition to mitralvalve replacement. Present experience is toosmall to allow definition of criteria for patientselection in terms of operability or choice ofprocedure. In the clinical setting beingdiscussed, the expected mortality with medicaltherapy is virtually 100%. If there is asignificant possibility of salvage with urgentsurgery, it obviously must be considered,particularly in the younger-aged patient.


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Ventricular Aneurysm andLeft Ventricular Wall Dyskinesia

Left ventricular aneurysm develops as acomplication of myocardial infarction in ap-proximately 10-15% of cases. The incidencedepends upon the extent and detail ofdiagnostic efforts made in each case. Withcombined electrocardiography, fluroscopy,and left ventriculography the incidence ofventricular aneurysm may be as high as20-25%.18 The aneurysm involves the anteriorwall and/or apex in 80% of cases and is usuallyassociated with an anterior infarction.65 Anacute aneurysm may develop in the earlypostinfarct period and be associated withcardiogenic shock, severe congestive heartfailure, recurrent ventricular arrhythmias, ornot contribute significantly to the patient'sclinical status.'7 18 Cardiogenic shock is morecommonly associated with a massive infarctwith loss of greater than 40% of the leftventricular wall.32 Clinical features and man-agement of this type of patient have beendiscussed previously. Frequently, a ventricularaneurysm is not clinically apparent for weeksor even months after infarction. The electro-cardiogram may demonstrate persistently ele-vated S-T segments during recovery frommyocardial infarction which should raise theclinical suspicion of ventricular aneurysm. Thecharacteristic S-T changes, inverted T waves,and persistent Q waves are present in 70-80%of patients with a clinically significant aneu-rysm.65The clinical features of left ventricular

aneurysm are usually those related to leftventricular dysfunction, particularly persistentcardiac failure.'17 18, 65, 66 Persistent or recur-rent ventricular arrhythmias, although rela-tively uncommon, may be the primary clinicalmanifestation of ventricular aneurysm.65' 67Occasionally, peripheral arterial thrombo-embolic complications may be the first indica-tion of a ventricular aneurysm. Layeredthrombus is nearly always present in ventricu-lar aneurysms and probably is responsible forthe majority of peripheral embolic complica-tions of myocardial infarction.The physiologic consequences of an acute


ventricular aneurysm in a nonischemic heartwere studied experimentally by Austen et al.68With a large ventricular aneurysm, there wasa marked depression in left ventricular strokework, cardiac output, and mean aortic arterialpressure. It is apparent that these changeswould be even more marked if significantmyocardial ischemia were present in additionto the mechanical effect of the aneurysm itself.The left ventricular ejection fraction decreasesand the left ventricular end-diastolic volumeincreases in the presence of an aneurysm or asignificant area of left ventricular akinesia.Recovery in performance of the left ventriclehas been shown to be not only related toimprovement in the ventricular ejection frac-tion and end-diastolic volume but also depen-dent upon the capacity for fiber shortening inadjacent myocardium.69 When there is in-volvement of greater than 25% of the leftventricular wall, the physiologic limit ofcompensatory myofibril shortening is reached,and maintenance of left ventricular strokevolume can be achieved only by increase inventricular volume (Starling mechanism ).53The natural history of large ventricular

aneurysms or areas of akinesis is usually thatof progressive and eventually intractable leftventricular failure. In a retrospective study,Shlichter, Hellerstein, and Katz70 found that73% of patients with left ventricular aneurysmsdied within 3 years and 88% within 5 years dueto heart failure, recurrent myocardial infarc-tion, or peripheral arterial embolization. Thestudy of Douglas, Sferazza, and Marici7'yielded similar results.

Surgical excision of a left ventricularaneurysm with cardiopulmonary bypass wasfirst achieved by Cooley et al.72 in 1958. Theprocedure has had extensive clinical applica-tion subsequently with an acceptably lowoperative mortality (5-15%) . The overallclinical results of aneurysm resection havebeen quite good. Favaloro et al.73 analyzed aseries of 130 patients undergoing ventricularaneurysm resection between 1959 and 1967.Complete follow-up ranging from severalmonths to 7 years was available in 68 patients.Forty-nine were living and 41 of this group

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were free of symptoms at the time of theirreport. When possible, surgical resection of aventricular aneurysm is delayed 3 months ormore following infarction in order to allowdemarcation of aneurysmal scar from that ofviable adjacent myocardium.As is true of all types of surgery for the

complications of coronary artery disease,resection of left ventricular aneurysm or largeakinetic areas is strictly palliative. The even-tual prognosis depends upon the course of theunderlying disease. 17 Recently there has beenincreasing enthusiasm for combing coronaryarterial revascularization with aneurysm orakinetic wall resection.59 74 This is trueparticularly for those patients who havesignificant angina in addition, which suggeststhe presence of ischemic myocardium inaddition to the inert scar of the aneurysm.74Whether direct coronary arterial revascular-ization can alter the natural course of coronaryartery disease remains unknown. Only thepassage of time and careful analysis of theresults of surgery can provide the answer.The socioeconomic implications of surgery

and overall care of the patient with life-threatening complications of acute myocardialinfarction present a major potential challengeto medical care delivery. Provision of ade-quate facilities, equipment, and trained per-sonnel to deal effectively with the problemsand therapeutic approaches outlined in thepreceeding pages will obviously be difficultoutside of major institutions that can absorbsizeable numbers of this type of critical carepatients, in addition to the many salvageablepatients requiring more conventional care.The problem is of such great magnitudesimply because of the large numbers ofpatients involved. An unpleasant, but never-theless pertinent, question is that related topriorities. Should hospitals, physicians, andpossibly the federal government devote largenumbers of highly trained personnel, facilities,time, and money to highly complex andperhaps overly heroic attempts to salvagepatients in an extremely high-risk group whendelivery of general medical care to the publicas a whole may not be entirely optimal? The

extensive time and personnel commitmentrequired in the care of these patients maysubtract subtly but recognizeably from thecare of eminently salvageable and rehabilita-table patients. An appropriate example is thegrowing volume of patients with symptomaticcoronary artery disease who must wait 3-4months for elective surgery due to the volumeload of patients undergoing cardiac surgery inmajor centers. The risk of the necessary delayin symptomatic patients awaiting surgery hasbeen estimated at a 3% mortality per month.Despite these considerations, it is exceedinglydifficult to deny any critically ill patientsuffering the effect of a complication ofmyocardial infarction the potential benefit ofsurgery, however small the chances of successare. The dilemma at present is not easilysoluble. The passage of time with a continuedaggressive approach to therapy balanced withcareful detailed analysis of the results shouldeventually provide the appropriate answers.

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CHARLES A. SANDERS and W. GERALD AUSTENELDRED D. MUNDTH, MORTIMER J. BUCKLEY, WILLARD M. DAGGETT,

Surgery for Complications of Acute Myocardial Infarction

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1972 American Heart Association, Inc. All rights reserved.

75231is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TXCirculation

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